Bronchopulmonary resistance to bacterial infection focuses principally on the alveolar macrophage phagocytic system; a truly nonspecific cellular defense mechanism responsible for the intrapulmonary inactivation of inhaled and aspirated organisms. Virus infections suppress the phagocytic capabilities of the alveolar macrophage and provide the basis by which bacterial infections become established and progress in the lung. Immunization with some bacterial species prevents the virus-induced defect and enhances the bactericidal capabilities of normal lungs while immunization with other organisms has no effect on abrogating the virus defect or enhancing resistance of non-virus infected lungs. This project is a study of the basic cellular mechanisms which focus on the alveolar macrophage system, its supporting immunologic apparatus, and viral-bacterial interactions of the lung. Specific projects are directed toward determining the immunologic apparatus of the lung and particularly the immune enhancement of pulmonary alveolar macrophage activity. The project is also directed to an understanding of the cellular basis of virus-bacterial interactions of the lung by studying how the immunologic apparatus prevents the virus induced defect, the role of the bacterial species, and the interaction between the variables (virus infection, immunity, and bacterial species) in the outcome of host resistance to bacterial infections of the lung.